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目的:为了研究I型糖尿病中细胞介导的自身免疫损伤因子。方法:采用有限稀释法建立糖尿病病人自身抗原IA2抗原特异性的T细胞克隆,51Cr释放细胞毒性试验测定T细胞激活的HLA限制性和IA2肽段中最小的抗原表位,并用流式细胞仪分析其表面凋亡相关的肿瘤坏死因子（Tumor Necrosis Factor,TNF）家族细胞因子Fas配体（Fas Ligand,FasL）、TNF凋亡诱导配体（Tumor Necrosis Factor Apoptosis-Inducing Ligand,TRAIL）、TNFα表达和细胞内的Perforin和Granzyme B的表达。结果:建立了IA2抗原特异性的T细胞克隆JDM IA2A2,其为HLA DR5限制,IA2最小抗原表位在IA2（838-846）,其表面没有 FasL表达,39.3％细胞表达TRAIL,29.23％细胞表达TNFα,细胞内没有Perforin,但59.16％细胞有Granzyme B。结论:TRAIL、TNFα、GranzymeB可能参与T细胞介导的胰岛β细胞损伤。
Purpose: To study cell-mediated autoimmune damage factors in type 1 diabetes. Methods: T-cell clones specific for IA2 antigen of diabetic patients were established by limiting dilution method. The 51Cr release cytotoxicity assay was used to determine the HLA-restricted T cell activation and the smallest epitope of IA2 peptide, and analyzed by flow cytometry The expression of Tumor Necrosis Factor (TNF) family of Fas ligand (FasL), Tumor necrosis factor Apoptosis-Inducing Ligand (TRAIL) Intracellular expression of Perforin and Granzyme B. Results: The IA2 antigen-specific T cell clone JDM IA2A2 was established, which was restricted by HLA DR5. The minimal epitope of IA2 was on IA2 (838-846), with no FasL on its surface, 39.3% on TRAIL and 29.23% TNFα, no Perforin in the cells, but 59.16% of the cells have Granzyme B. Conclusion: TRAIL, TNFα, GranzymeB may be involved in T cell-mediated islet β cell injury.